Microbiology · MU Sofia

90. Family Coronaviridae – SARS Virus

Covers the Coronaviridae family and the SARS coronavirus, starting with general features such as the viral envelope, RNA genome, crown-like spikes and transmission routes. It then moves through morphology and structural proteins, virulence factors, pathogenesis, clinical features with complications and mortality, diagnosis, treatment and prevention. A summary table closes the note, giving an overview of the SARS-CoV-1 virus.

Inside: 5 sections · 4 labelled pictures · 2 tables · 14 flashcards · 3 min

Topic 90 of 113 in the MU Sofia syllabus for Microbiology (Medicine, Year 3). The free AceMed note covers it in 5 sections, about 316 words (3 min of reading), with 14 flashcards.

In this note

  1. Family Coronaviridae – SARS Virus
  2. I. General Characteristics
  3. II. Morphology and Structure
  4. III. SARS Virus (Severe Acute Respiratory Syndrome Coronavirus – SARS-CoV-1)
  5. IV. Summary Table – SARS-CoV-1 Overview

I. General Characteristics

  • Coronaviridae are enveloped, positive-sense, single-stranded RNA viruses.
  • Genome is non-segmented, largest among RNA viruses (~30 kb).
  • Helical nucleocapsid, replicates in cytoplasm.
  • Named for the “crown-like” (corona) appearance due to surface spike (S) glycoproteins.
  • Transmission is mainly through respiratory droplets, direct contact, and aerosolized secretions.
  • Reservoir: Bats (natural host), with intermediate hosts like civet cats in zoonotic SARS-CoV-1.

III. SARS Virus (Severe Acute Respiratory Syndrome Coronavirus – SARS-CoV-1)

A. Virulence Factors

  • Spike (S) protein:
  • Binds to ACE2 receptor (mainly in lungs, intestine, kidney).
  • Triggers fusion and entry → defines tissue tropism and host range.
  • Envelope (E) protein:
  • Facilitates virus budding and release; contributes to inflammation.
  • Accessory proteins:
  • Interfere with host interferon signaling, delaying immune response.
  • Nucleocapsid (N):
  • Enhances viral RNA synthesis; modulates host cell stress responses.
  • Downregulation of ACE2:
  • Leads to imbalance in the renin-angiotensin system → lung injury.

B. Pathogenesis

  • Initial entry via respiratory epithelium → virus uses ACE2 receptor to enter cells.
  • Replication in epithelial cells causes cytopathic effects, apoptosis, and inflammation.
  • Systemic spread can involve:
  • Lungs: diffuse alveolar damage → ARDS (Acute Respiratory Distress Syndrome)
  • GI tract: diarrhea (virus found in stool)
  • Immune system: cytokine storm in severe cases → multiorgan failure.

C. Clinical Features

  • Incubation period: 2–10 days.
  • Symptoms:
  • High fever (>38°C), dry cough, malaise
  • Dyspnea (within ~1 week), diarrhea (20–25%)
  • No coryza (runny nose is rare, unlike common cold)
  • Severe complications:
  • ARDS, respiratory failure, need for ventilation
  • Secondary bacterial pneumonia
  • High mortality (~10%, higher in elderly)

D. Diagnosis

  • RT-PCR: gold standard (detects viral RNA in respiratory samples).
  • Serology: detection of antibodies (IgM/IgG) for retrospective diagnosis.
  • Chest imaging:
  • Ground-glass opacities, bilateral infiltrates (similar to COVID-19).
  • Viral culture: possible but high biohazard risk.

E. Treatment

  • No proven antiviral; treatment is supportive:
  • Oxygen, mechanical ventilation
  • Corticosteroids used cautiously
  • Investigational drugs: interferons, lopinavir/ritonavir (limited success)

F. Prevention and Control

  • No licensed vaccine for SARS-CoV-1.
  • Control measures:
  • Isolation, quarantine of contacts
  • Strict infection control in hospitals
  • Travel screening and surveillance
  • Lessons from SARS guided later COVID-19 responses.

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